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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

MnBP     2-butoxycarbonylbenzoic acid

Synonyms: SureCN151027, NSC-8479, HMDB13247, NSC8479, AK-57667, ...
 
 
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Disease relevance of AI3-01768

 

High impact information on AI3-01768

  • However, mEP and mBP showed positive correlations with SHBG (r = 0.323, p = 0.002 and r = 0.272, p = 0.01, respectively); mMP, mEP, and mBP with LH:free testosterone ratio (r = 0.21-0.323, p = 0.002-0.044) and miNP with luteinizing hormone (r = 0.243, p = 0.019). mBP was negatively correlated with free testosterone (r = -0.22, p = 0.033) [3].
  • For below-reference sperm motility, there was also a greater than additive interaction between monobutyl phthalate (MBP) and PCB-153 (RERI = 1.42; 95% CI, 0.09-3.76) and CYP450-inducing PCBs (RERI = 1.87; 95% CI, 0.56-4.52) and a suggestive interaction between MBP and sum of PCBs (RERI = 1.35; 95% CI, -0.11 to 3.48) [4].
  • From HPLC analyses, it was shown that unchanged DBP and its metabolites mono-n-butyl phthalate (MBP) and MBP glucuronide were rapidly transferred to the embryonic tissues, where their levels were constantly lower than those in maternal plasma [5].
  • The objective of this study was to evaluate the pharmacokinetics of MBP and monobutyl phthalate glucuronide (MBP-G) in pregnant rats following intravenous (i.v.) dosing with MBP [2].
  • Results were consistent with two previous studies that utilized oral doses of DBP, suggesting that chemical (DBP versus MBP), vehicle (oil versus aqueous), dose level, and route (oral versus i.v.) have minimal effects on the maternal pharmacokinetics of MBP and MBP-G [2].
 

Biological context of AI3-01768

  • This study provides direct pharmacokinetic analysis for MBP and MBP-G in pregnant rats during fetal male reproductive development, and indicates that future pharmacokinetic or toxicology studies can reliably utilize oral dosing with DBP [2].
  • Immature testes may thus be more sensitive to MBP, which induces the germ cell apoptosis in seminiferous tubules and testicular atrophy in prepubertal young rats [6].
 

Anatomical context of AI3-01768

  • In 20-day-old fetuses (n = 15), the degree of transabdominal testicular ascent in relation to the bladder neck was thus found to be significantly higher in MBP-treated rats than that of the controls (n = 19) [1].
  • It is therefore suggested that prenatal exposure to MBP may disturb the Sertoli cells and elevate the fetal testes relative to the bladder neck while also inducing cryptorchidism postnatally [1].
  • In addition, the frequency of an apoptotic cell appearance in the seminiferous tubules was determined in both MBP-treated and control groups [6].
  • High-doses of MBP are thus considered to inhibit the transabdominal descent of the testis, probably due to its estrogenic activity, whereas low-doses of MBP may act as an anti-androgen and thereby inhibit inguinoscrotal testicular descent in postnatal rats [7].
  • A histological examination of the MBP-treated testes showed a decreased seminiferous tubular diameter and an inhibited maturation of germ cells in comparison to those of the control testes [6].
 

Associations of AI3-01768 with other chemical compounds

  • As metabolites by the crude enzyme solutions, DMP, MBP and an unknown diester derivative were produced from DBP [8].
  • DMP, DEP, monomethyl phthalate, monobutyl phthalate (MBP) and an unknown diester were produced from DBP [8].
 

Gene context of AI3-01768

  • These findings support the hypothesis that MBP, a potent teratogen, largely contributes to the embryotoxic effects of DBP [5].
  • Di-n-butyl phthalate (DBP) appears to be a ubiquitous environmental contaminant, as indicated by its presence in air, water, and soil worldwide (Giam et al., 1980; ATSDR, 2001; Peterson & Freeman, 1982) and the presence of its major metabolite, monobutyl phthalate (MBP), in random human urine samples (Blount et al., 2000) [9].
 

Analytical, diagnostic and therapeutic context of AI3-01768

References

  1. Prenatal phthalate causes cryptorchidism postnatally by inducing transabdominal ascent of the testis in fetal rats. Imajima, T., Shono, T., Zakaria, O., Suita, S. J. Pediatr. Surg. (1997) [Pubmed]
  2. Pharmacokinetics of monobutylphthalate, the active metabolite of di-n-butylphthalate, in pregnant rats. Kremer, J.J., Williams, C.C., Parkinson, H.D., Borghoff, S.J. Toxicol. Lett. (2005) [Pubmed]
  3. Human breast milk contamination with phthalates and alterations of endogenous reproductive hormones in infants three months of age. Main, K.M., Mortensen, G.K., Kaleva, M.M., Boisen, K.A., Damgaard, I.N., Chellakooty, M., Schmidt, I.M., Suomi, A.M., Virtanen, H.E., Petersen, D.V., Andersson, A.M., Toppari, J., Skakkebaek, N.E. Environ. Health Perspect. (2006) [Pubmed]
  4. Evidence of interaction between polychlorinated biphenyls and phthalates in relation to human sperm motility. Hauser, R., Williams, P., Altshul, L., Calafat, A.M. Environ. Health Perspect. (2005) [Pubmed]
  5. Assessment of the developmental toxicity, metabolism, and placental transfer of Di-n-butyl phthalate administered to pregnant rats. Saillenfait, A.M., Payan, J.P., Fabry, J.P., Beydon, D., Langonne, I., Gallissot, F., Sabate, J.P. Toxicol. Sci. (1998) [Pubmed]
  6. Age-specific effect of phthalate ester on testicular development in rats. Kondo, T., Shono, T., Suita, S. J. Pediatr. Surg. (2006) [Pubmed]
  7. Dose-dependent effect of phthalate ester on testicular descent in pre-and post natal rats. Shono, T., Suita, S. Urol. Res. (2003) [Pubmed]
  8. Phthalate esters detected in various water samples and biodegradation of the phthalates by microbes isolated from river water. Hashizume, K., Nanya, J., Toda, C., Yasui, T., Nagano, H., Kojima, N. Biol. Pharm. Bull. (2002) [Pubmed]
  9. Exposure to low concentrations of di-n-butyl phthalate during embryogenesis reduces survivability and impairs development of Xenopus laevis frogs. Lee, S.K., Owens, G.A., Veeramachaneni, D.N. J. Toxicol. Environ. Health Part A (2005) [Pubmed]
  10. Differences in urinary metabolic profile from di-n-butyl phthalate-treated rats and hamsters. A possible explanation for species differences in susceptibility to testicular atrophy. Foster, P.M., Cook, M.W., Thomas, L.V., Walters, D.G., Gangolli, S.D. Drug Metab. Dispos. (1983) [Pubmed]
 
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